Medicine:Vein graft failure

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Short description: Blockage of a grafted vein

In medicine, vein graft failure (VGF) is a condition in which vein grafts, which are used as alternative conduits in bypass surgeries (e.g. CABG), get occluded.

Veins, mainly the great saphenous vein (GSV) are the most frequently used conduits in bypass surgeries (CABG or PABG), due to their ease of use and availability.[1] Some structural changes of intima thickening and vein wall remodeling are necessary for vein graft adaptation to the arterial environment. The reasons why some of the grafts progress to clinical stenosis is unknown. The patency rates of saphenous vein grafts after CABG at 1 year is approximately 80%.[2][3] After 5 years the patency rate drops to 65% and at 10 years GSV patency rates are approximately 50%, with only half of the veins are atherosclerosis free.[4] VGF may be identified in asymptomatic patients, but can also produce symptoms of ischemia, depending on the area of the supplied territory of the heart, and the function of native arteries and other grafts. VGF has been closely correlated with revascularization, myocardial infarction and death.[2][5] Treatment of occluded GSVs can be performed by percutaneous coronary intervention or redo CABG and is considered to be challenging, and thus preventing their obstruction is of great importance.[6]

Mechanism

During and after the harvesting, veins go through a period of ischemia and reperfusion after engraftment, which causes damage to endothelial and smooth muscle cells (SMC).[7] The grafting exposes the vein to arterial pressure and flow that causes increased shear stress and wall tension, which further damages the endothelial layer and SMC.[8] The damage causes local release of tissue factors and reduced bioavailability of prostacyclin and nitric oxide (NO), all of which contribute to platelet activation, deposition of fibrin, which promotes thrombosis.[9] Growth factors that released from macrophages and platelets lead to increased proliferation and migration of SMCs to the intima. The migrated SMC release extracellular matrix resulting in reduced intimal cellularity.[10] Low levels of endothelial nitric oxide, adenosine and prostaglandins, further contribute to SMC proliferation.[11][12][13] Over time continued SMC migration and proliferation cause extracellular matrix deposition and fibrotic change that lead to development of intimal hyperplasia, which results in luminal loss that makes the graft more susceptible to atherosclerosis.[14] Progressive atherosclerosis is the primarily cause of late vein graft failure. Vein graft atherosclerotic lesions are more diffuse and concentric, yet less calcified, compared to native atherosclerotic lesions, and are more susceptible to thrombosis formation and rupture.[15]

Graft failure depending on saphenous vein harvesting technique

Having an intact outer fat pedicle is what differentiates the two main techniques for harvesting saphenous vein grafts. Conventionally, the outer fat pedicle is removed during the harvesting process. It has been proposed that the no-touch technique, leaving the outer fat pedicle intact, will cause less endothelial damage at the time of harvest.[16] This lessens intimal hyperplasia in the long run.[17]

Prevention

Statins and antiplatelets such as aspirin, are the only medications recommended by the ESC guidelines and the ACC/AHA Task Force guidelines for the prevention of VGF.[18][19][20][21] Different surgical techniques had been studied in attempt to reduce VGF. The No-touch technique is where the vein is harvested with the surrounding tissues, keeping the vasa vasorum and the nerves in the adventitia intact. This technique shown to improve vein graft patency and less development of intimal hyperplasia.[22][23] Despite the benefits shown, the use of No-touch technique in CABG is limited to a few centers. Probably because of the shift toward improved cosmetic outcome and patient satisfaction provided by endoscopic vein harvesting (EVH).[24] Although, EVH has been associated with higher risk of vein graft stenosis and occlusion.[25] The solutions in which vein grafts are stored after harvesting also play an important role. Buffered saline, instead of saline or blood, has shown to reduce the risk of significant stenosis or occlusion.[26] Providing the vein with external support prior to grafting has shown to reduce intimal hyperplasia formation and improve the hemodynamics within the graft.[27][28][29] Gene therapy is another strategy that been suggested to prevent VGF as the veins are ideally suited for ex vivo treatment prior to grafting. Preclinical studies showed that such strategy has the potential to reduce intimal hyperplasia but more clinical data is needed.[30][31][32][33]

References

  1. ↑ "Long-term patency of saphenous vein and left internal mammary artery grafts after coronary artery bypass surgery: results from a Department of Veterans Affairs Cooperative Study". J. Am. Coll. Cardiol. 44 (11): 2149–56. December 2004. doi:10.1016/j.jacc.2004.08.064. PMID 15582312. 
  2. ↑ 2.0 2.1 Fitzgibbon, GM; Kafka, HP; Leach, AJ; Keon, WJ; Hooper, GD; Burton, JR (September 1996). "Coronary bypass graft fate and patient outcome: angiographic follow-up of 5,065 grafts related to survival and reoperation in 1,388 patients during 25 years.". Journal of the American College of Cardiology 28 (3): 616–26. doi:10.1016/0735-1097(96)00206-9. PMID 8772748. 
  3. ↑ "Saphenous vein graft failure after coronary artery bypass surgery: insights from PREVENT IV". Circulation 130 (17): 1445–51. October 2014. doi:10.1161/CIRCULATIONAHA.113.008193. PMID 25261549. 
  4. ↑ "Management and Prevention of Saphenous Vein Graft Failure: A Review". Cardiol Ther 6 (2): 203–223. December 2017. doi:10.1007/s40119-017-0094-6. PMID 28748523. 
  5. ↑ "Relation of early saphenous vein graft failure to outcomes following coronary artery bypass surgery". Am. J. Cardiol. 96 (9): 1254–9. November 2005. doi:10.1016/j.amjcard.2005.06.067. PMID 16253593. 
  6. ↑ "Clinical presentation and angiographic characteristics of saphenous vein graft failure after stenting: insights from the SOS (stenting of saphenous vein grafts) trial". JACC Cardiovasc Interv 2 (9): 855–60. September 2009. doi:10.1016/j.jcin.2009.06.014. PMID 19778774. 
  7. ↑ Lardenoye, JH; de Vries, MR; Löwik, CW; Xu, Q; Dhore, CR; Cleutjens, JP; van Hinsbergh, VW; van Bockel, JH et al. (4 October 2002). "Accelerated atherosclerosis and calcification in vein grafts: a study in APOE*3 Leiden transgenic mice.". Circulation Research 91 (7): 577–84. doi:10.1161/01.res.0000036901.58329.d7. PMID 12364385. 
  8. ↑ Angelini, GD; Passani, SL; Breckenridge, IM; Newby, AC (December 1987). "Nature and pressure dependence of damage induced by distension of human saphenous vein coronary artery bypass grafts.". Cardiovascular Research 21 (12): 902–7. doi:10.1093/cvr/21.12.902. PMID 3502670. 
  9. ↑ Manchio, JV; Gu, J; Romar, L; Brown, J; Gammie, J; Pierson RN, 3rd; Griffith, B; Poston, RS (June 2005). "Disruption of graft endothelium correlates with early failure after off-pump coronary artery bypass surgery.". The Annals of Thoracic Surgery 79 (6): 1991–8. doi:10.1016/j.athoracsur.2004.12.054. PMID 15919298. 
  10. ↑ Allaire, E; Clowes, AW (February 1997). "Endothelial cell injury in cardiovascular surgery: the intimal hyperplastic response.". The Annals of Thoracic Surgery 63 (2): 582–91. doi:10.1016/S0003-4975(96)01045-4. PMID 9033355. 
  11. ↑ Nwasokwa, ON (1 October 1995). "Coronary artery bypass graft disease.". Annals of Internal Medicine 123 (7): 528–45. doi:10.7326/0003-4819-123-7-199510010-00009. PMID 7661498. 
  12. ↑ Schwartz, SM; deBlois, D; O'Brien, ER (September 1995). "The intima. Soil for atherosclerosis and restenosis.". Circulation Research 77 (3): 445–65. doi:10.1161/01.res.77.3.445. PMID 7641318. 
  13. ↑ Zhang, L; Peppel, K; Brian, L; Chien, L; Freedman, NJ (December 2004). "Vein graft neointimal hyperplasia is exacerbated by tumor necrosis factor receptor-1 signaling in graft-intrinsic cells.". Arteriosclerosis, Thrombosis, and Vascular Biology 24 (12): 2277–83. doi:10.1161/01.ATV.0000147766.68987.0d. PMID 15486311. 
  14. ↑ Stary, HC; Blankenhorn, DH; Chandler, AB; Glagov, S; Insull W, Jr; Richardson, M; Rosenfeld, ME; Schaffer, SA et al. (January 1992). "A definition of the intima of human arteries and of its atherosclerosis-prone regions. A report from the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association.". Circulation 85 (1): 391–405. doi:10.1161/01.cir.85.1.391. PMID 1728483. 
  15. ↑ Yahagi, K; Kolodgie, FD; Otsuka, F; Finn, AV; Davis, HR; Joner, M; Virmani, R (February 2016). "Pathophysiology of native coronary, vein graft, and in-stent atherosclerosis.". Nature Reviews. Cardiology 13 (2): 79–98. doi:10.1038/nrcardio.2015.164. PMID 26503410. 
  16. ↑ Ramos De Souza, Domingos; Dashwood, Michael R.; Samano, Ninos (October 2017). "Saphenous vein graft harvesting and patency: No-touch harvesting is the answer" (in en). The Journal of Thoracic and Cardiovascular Surgery 154 (4): 1300–1301. doi:10.1016/j.jtcvs.2017.02.010. PMID 28918921. 
  17. ↑ Samano, Ninos; Souza, Domingos; Dashwood, Michael R (June 2021). "Saphenous veins in coronary artery bypass grafting need external support" (in en). Asian Cardiovascular and Thoracic Annals 29 (5): 457–467. doi:10.1177/0218492320980936. ISSN 0218-4923. PMID 33307718. 
  18. ↑ Authors/Task Force, members.; Windecker, S; Kolh, P; Alfonso, F; Collet, JP; Cremer, J; Falk, V; Filippatos, G et al. (1 October 2014). "2014 ESC/EACTS Guidelines on myocardial revascularization: The Task Force on Myocardial Revascularization of the European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS)Developed with the special contribution of the European Association of Percutaneous Cardiovascular Interventions (EAPCI).". European Heart Journal 35 (37): 2541–619. doi:10.1093/eurheartj/ehu278. PMID 25173339. 
  19. ↑ "2011 ACCF/AHA Guideline for Coronary Artery Bypass Graft Surgery: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines". Circulation 124 (23): e652–735. December 2011. doi:10.1161/CIR.0b013e31823c074e. PMID 22064599. 
  20. ↑ European Stroke, Organisation.; Tendera, M; Aboyans, V; Bartelink, ML; Baumgartner, I; Clément, D; Collet, JP; Cremonesi, A et al. (November 2011). "ESC Guidelines on the diagnosis and treatment of peripheral artery diseases: Document covering atherosclerotic disease of extracranial carotid and vertebral, mesenteric, renal, upper and lower extremity arteries: the Task Force on the Diagnosis and Treatment of Peripheral Artery Diseases of the European Society of Cardiology (ESC).". European Heart Journal 32 (22): 2851–906. doi:10.1093/eurheartj/ehr211. PMID 21873417. 
  21. ↑ Anderson, JL; Halperin, JL; Albert, NM; Bozkurt, B; Brindis, RG; Curtis, LH; DeMets, D; Guyton, RA et al. (2 April 2013). "Management of patients with peripheral artery disease (compilation of 2005 and 2011 ACCF/AHA guideline recommendations): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines.". Circulation 127 (13): 1425–43. doi:10.1161/CIR.0b013e31828b82aa. PMID 23457117. 
  22. ↑ Souza, DS; Dashwood, MR; Tsui, JC; Filbey, D; Bodin, L; Johansson, B; Borowiec, J (April 2002). "Improved patency in vein grafts harvested with surrounding tissue: results of a randomized study using three harvesting techniques.". The Annals of Thoracic Surgery 73 (4): 1189–95. doi:10.1016/s0003-4975(02)03425-2. PMID 11996262. 
  23. ↑ Souza, DS; Johansson, B; Bojö, L; Karlsson, R; Geijer, H; Filbey, D; Bodin, L; Arbeus, M et al. (August 2006). "Harvesting the saphenous vein with surrounding tissue for CABG provides long-term graft patency comparable to the left internal thoracic artery: results of a randomized longitudinal trial.". The Journal of Thoracic and Cardiovascular Surgery 132 (2): 373–8. doi:10.1016/j.jtcvs.2006.04.002. PMID 16872965. 
  24. ↑ "Endoscopic Versus "No-Touch" Saphenous Vein Harvesting for Coronary Artery Bypass Grafting: A Trade-Off Between Wound Healing and Graft Patency". Angiology 67 (2): 121–32. February 2016. doi:10.1177/0003319715584126. PMID 25972395. 
  25. ↑ Deppe, AC; Liakopoulos, OJ; Choi, YH; Slottosch, I; Kuhn, EW; Scherner, M; Stange, S; Wahlers, T (March 2013). "Endoscopic vein harvesting for coronary artery bypass grafting: a systematic review with meta-analysis of 27,789 patients.". The Journal of Surgical Research 180 (1): 114–24. doi:10.1016/j.jss.2012.11.013. PMID 23218736. 
  26. ↑ Harskamp, RE; Alexander, JH; Schulte, PJ; Brophy, CM; Mack, MJ; Peterson, ED; Williams, JB; Gibson, CM et al. (August 2014). "Vein graft preservation solutions, patency, and outcomes after coronary artery bypass graft surgery: follow-up from the PREVENT IV randomized clinical trial.". JAMA Surgery 149 (8): 798–805. doi:10.1001/jamasurg.2014.87. PMID 25073921. 
  27. ↑ Taggart, DP; Ben Gal, Y; Lees, B; Patel, N; Webb, C; Rehman, SM; Desouza, A; Yadav, R et al. (June 2015). "A Randomized Trial of External Stenting for Saphenous Vein Grafts in Coronary Artery Bypass Grafting.". The Annals of Thoracic Surgery 99 (6): 2039–45. doi:10.1016/j.athoracsur.2015.01.060. PMID 25886810. http://spiral.imperial.ac.uk/bitstream/10044/1/53822/2/ATS-2014-472654v2-Orion_accepted.pdf. 
  28. ↑ "A prospective study of external stenting of saphenous vein grafts to the right coronary artery: the VEST II study". Eur J Cardiothorac Surg 51 (5): 952–958. May 2017. doi:10.1093/ejcts/ezw438. PMID 28379404. 
  29. ↑ Meirson, T; Orion, E; Di Mario, C; Webb, C; Patel, N; Channon, KM; Ben Gal, Y; Taggart, DP (October 2015). "Flow patterns in externally stented saphenous vein grafts and development of intimal hyperplasia.". The Journal of Thoracic and Cardiovascular Surgery 150 (4): 871–8. doi:10.1016/j.jtcvs.2015.04.061. PMID 26242834. 
  30. ↑ Eefting, D; de Vries, MR; Grimbergen, JM; Karper, JC; van Bockel, JH; Quax, PH (February 2010). "In vivo suppression of vein graft disease by nonviral, electroporation-mediated, gene transfer of tissue inhibitor of metalloproteinase-1 linked to the amino terminal fragment of urokinase (TIMP-1.ATF), a cell-surface directed matrix metalloproteinase inhibitor.". Journal of Vascular Surgery 51 (2): 429–37. doi:10.1016/j.jvs.2009.09.026. PMID 20036101. 
  31. ↑ Quax, PH; Lamfers, ML; Lardenoye, JH; Grimbergen, JM; de Vries, MR; Slomp, J; de Ruiter, MC; Kockx, MM et al. (30 January 2001). "Adenoviral expression of a urokinase receptor-targeted protease inhibitor inhibits neointima formation in murine and human blood vessels.". Circulation 103 (4): 562–9. doi:10.1161/01.cir.103.4.562. PMID 11157723. 
  32. ↑ Karper, JC; de Vries, MR; van den Brand, BT; Hoefer, IE; Fischer, JW; Jukema, JW; Niessen, HW; Quax, PH (May 2011). "Toll-like receptor 4 is involved in human and mouse vein graft remodeling, and local gene silencing reduces vein graft disease in hypercholesterolemic APOE*3Leiden mice.". Arteriosclerosis, Thrombosis, and Vascular Biology 31 (5): 1033–40. doi:10.1161/ATVBAHA.111.223271. PMID 21330606. 
  33. ↑ Pradhan-Nabzdyk, L; Huang, C; LoGerfo, FW; Nabzdyk, CS (September 2014). "Current siRNA targets in the prevention and treatment of intimal hyperplasia.". Discovery Medicine 18 (98): 125–32. PMID 25227753. 



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